Heart Failure

HEART FAILURE

An increasing number of patients present for sur-gery with either systolic and/or diastolic heart failure. Congestive heart failure affects more than 5 million Americans. Heart failure may be second-ary to ischemia, valvular heart disease, infectious agents, and many types of cardiomyopathy. Most patients seek medical attention secondary to heart failure because of complaints of dyspnea and fatigue. Heart failure develops over time, as symptoms worsen (Figure 21–5). Patients generally undergo echocardiography to diagnose structural heart defects, to detect signs of cardiac “remodeling”, to determine the left ventricular ejection fraction, and to assess the heart’s diastolic function. Laboratory evaluations of concentration of brain natriuretic peptide (BNP) are likewise obtained to distinguish heart failure from other causes of dyspnea. BNP is released from the heart, and its elevation is associ-ated with impaired ventricular function.In response to ventricular failure, the body attempts to compensate for LV systolic function through the sympathetic and renin–angiotensin– aldosterone system. Consequently, patients experi-ence salt retention, volume expansion, sympathetic stimulation, and vasoconstriction. The heart dilates to maintain the stroke volume in spite of decreased contractility. Over time, compensatory mecha-nisms fail and contribute to the symptoms asso-ciated with heart failure (eg, edema, tachycardia, decreased tissue perfusion). Patients with systolic heart failure are likely to present to surgery hav-ing been previously treated with diuretics, ACE inhibitors, angiotensin receptor blockers, and

possibly aldosterone antagonists. Electrolytes must be measured, as heart failure therapies frequently lead to changes in serum potassium concentration. Angiotensin receptor blocker or ACE inhibitor use may contribute to periinduction hypotension in the patient with heart failure. ACE inhibitors are rarely associated with angioedema requiring emergent airway management.

Diastolic ventricular dysfunction pro-duces symptoms of congestion and heart failure. Myocardial relaxation is a dynamic, not passive, process. The heart with preserved diastolic func-tion accommodates volume during diastole, with minimal increases in left ventricular end-diastolic pressure. Conversely, the heart with diastolic dys-function relaxes poorly and produces increased left ventricular end-diastolic pressure. The left ven-tricular end-diastolic pressure is transmitted to the left atrium and pulmonary vasculature resulting in symptoms of congestion.

Anesthetic management of the patient with heart failure requires careful assessment and opti-mization of intravascular fluid volume—especially if positive inotropic agents, vasoconstrictors, or vasodilators are used. In particular, patients with diastolic dysfunction may tolerate increases in volume poorly, leading to pulmonary congestion.